What is urine analysis?
 Urine analysis, also called
Urinalysis – one of the oldest
laboratory procedures in the
practice of medicine.
 Also knows as Urine-R&M
(routine & microscopy)
 Is an array of tests performed on
urine, and one of the most
common methods of medical
diagnosis.
Courtesy of the National Library of Medicine
Why urinalysis?
 General evaluation of health
 Diagnosis of disease or disorders of the kidneys or
urinary tract
 Diagnosis of other systemic disease that affect kidney
function
 Monitoring of patients with diabetes
 Screening for drug abuse (eg. Sulfonamide or
aminoglycosides)
Collection of urine specimens
 Improper collection---- may invalidate the
results
 Containers for collection of urine should be
wide mouthed, clean and dry.
 Analysed within 2 hours of collection else
requires refrigeration.
Types of urine sample
Sample type Sampling Purpose
Random specimen No specific time
most common, taken anytime of
day
Routine screening, chemical &
FEME
Morning sample First urine in the morning,
most concentrated
Pregnancy test, microscopic test
Clean catch midstream Discard first few ml, collect the
rest
Culture
24 hours All the urine passed during the
day and night and next day Ist
sample is collected.
used for quantitative and
qualitative analysis of substances
Postprandial 2 hours after meal Determine glucose in diabetic
monitoring
Supra-pubic aspired Needle aspiration Obtaining sterile urine
a
c
b
a: clean catch urine collection
method
in children
b: Suprapubic aspiration of urine.
c: Urine storage and transportation
kit
Urinalysis ;What to look for?
 Urinalysis consists of the following measurements:
 Macroscopic or physical examination
 Chemical examination
 Microscopic examination of the sediment
 Urine culture
Physical examination of urine
Examination of physical
characteristics:
 Volume
 Color
 Odor
 pH and
 Specific gravity
 The refractometer or a reagent strip is used to
measure specific gravity
Physical examination continued…
 Normal- 1-2.5 L/day
 Oliguria- Urine Output < 400ml/day
Seen in
 Dehydration
 Shock
 Acute glomerulonephritis
 Renal Failure
 Polyuria- Urine Output > 2.5 L/day
Seen in
 Increased water ingestion
 Diabetes mellitus and insipidus.
 Anuria- Urine output < 100ml/day
Seen in renal shut down
Volume
 Normal- pale yellow in color due to pigments
urochrome, urobilin and uroerythrin.
 Cloudiness may be caused by excessive
cellular material or protein, crystallization or
precipitation of non pathological salts upon
standing at room temperature or in the
refrigerator.
 Colour of urine depending upon it’s constituents.

Color
Physical examination continued…
 Abnormal colors:
 Colorless – diabetes, diuretics.
 Deep Yellow – concentrated urine,
excess bile pigments, jaundice
Color
Pathological Non pathological
White Chyle
Pus
Phosphates
Yellow to
Orange
Bilirubin
Urobilin
Concentrated urine
Carrots
Senna
Riboflavin
Acriflavine
sulfasalazine
Pink to Red Haemoglobin
Myoglobin
Porphyrins
Red blood cells
Beets(anthocynin)
Aminopyrine
Methyldopa
Food color
Bromosulfonphthalein
Pyridium
Senna
Pathological Nonpathological
Red to Brown to
Purple
Porphobilinogen
Uroporphyrin
Brown to Black Homogenistic acid
Melanin
Myoglobin
Methaemoglobin
Phenol
Porphyrins
Chloroquine
Iron compounds
Levodopa
Metronidazole
Quinine
Blue to Green Biliverdin
Pseudomonas infection
Acriflavine
AzureA
Methylene blue
Vit B
Phenyl salicylate
Amitryptiline
ODOUR
 Fruity/sweet odour- presence of ketones.
 Pungent smell- presence of bacteria/ specimen contaminated
with bacteria.
 Sweaty feet- Isolvaleric acidemia
 Misty/mousy odour- Phenylketonuria.
 Maple syrup- Congenital metabolic disorder.
 Fishy odour/Rancid butter- Hypermethioninemia
pH
 Concentration ability of kidney to maintain normal hydrogen ion
concentration
 Normal pH – 4.6 to 8.0
 Average- 6.0
 PROCEDURE
 Dip the litmus paper strips in the urine, remove and read the
color change immediately.
 Blue litmus turns red – acid
 Red litmus turns blue – alkaline
 Decrease in pH
 High protein intake
 Ingestion of cranberries
 Respiratory acidosis
 Metabolic acidosis
 Uremia
 Severe diarrhoea
 Starvation
 UTI caused by E.coli
 Increase in pH
 Diet high in vegetables and
citrus fruits
 Respiratory alkalosis
 Metabolic alkalosis
 Vomiting
 UTI caused by Proteus and
Pseudomonas
 Reflects ability of kidney to maintain normal hydrogen
ion concentration in plasma & ECF
 Urine pH ranges from 4.5 to 8
 Normally it is slightly acidic lying between 6 – 6.5.
 Tested by:
 litmus paper
 pH paper
 dipsticks
 Acidic Urine –Ketosis (diabetes, starvation,
fever),systemic acidosis, UTI- E.coli, acidification
therapy
 Alkaline Urine – after meal, systemic alkalosis, UTI –
proteus, alkalization therapy
pH
 It is measurement of urine density which reflects the
ability of the kidney to concentrate or dilute the urine
relative to the plasma from which it is filtered.
 Measured by:
 urinometer
 refractometer
 dipsticks
Specific gravity
 Normal :- 1.001- 1.040.
 Increase in Specific Gravity - Low water intake, Diabetes
mellitus, Albuminuruia, Acute nephritis.
 Decrease in Specific Gravity - Absence of ADH, Renal
Tubular damage.
 Fixed specific gravity (isosthenuria)=1.010
Specific gravity
Microscopic examination of urine
 A sample of well-mixed urine (usually 10-15 ml) is
centrifuged in a test tube at relatively low speed (about 2000-
3,000 rpm) for 5-10 minutes which produces a
concentration of sediment (cellular matter) at the bottom of
the tube.
 A drop of sediment is poured onto a glass slide, a thin slice of
glass (a coverslip) is place over it ond observed under
microscope
Microscopic examination of urine
 A variety of normal and abnormal cellular elements may be
seen in urine sediment such as:
 Red blood cells
 White blood cells
 Mucus
 Various epithelial cells
 Various crystals
 Bacteria
 Casts
 Per High Power Field (HPF) (400x)
 > 3 erythrocytes
 > 5 leukocytes
 > 2 renal tubular cells
 > 10 bacteria
 Per Low Power Field (LPF) (200x)
 > 3 hyaline casts or > 1 granular cast
 > 10 squamous cells (indicative of contaminated specim
 Any other cast (RBCs, WBCs)
 Presence of:
 Fungal hyphae or yeast, parasite, viral inclusions
 Pathological crystals (cystine, leucine, tyrosine)
 Large number of uric acid or calcium oxalate crystals
Abnormal findings
Microscopic examination of urine
 Hematuria is the presence of abnormal numbers of red
cells in urine due to any of several possible causes.
 glomerular damage,
 tumors which erode the urinary tract anywhere along its
length,
 kidney trauma,
 urinary tract stones,
 acute tubular necrosis,
 upper and lower urinary tract infections,
 nephrotoxins
 WBC in high numbers indicate inflammation or infection
somewhere along the urinary or genital tract
Microscopic examination of urine
Red blood cells in urine appear as refractile disks White blood cells in urine
Microscopic examination of urine
Casts
 Urinary casts are cylindrical aggregations of particles that
form in the distal nephron, dislodge, and pass into the urine.
In urinalysis they indicate kidney disease.
 They form via precipitation ofTamm-Horsfall mucoprotein
which is secreted by renal tubule cells.
Microscopic examination of urine
Types of cast seen :
 Acellular cast: Hyaline casts, Granular casts, Waxy casts,
Fatty casts, Pigment casts, Crystal casts.
 Cellular cast: Red cell casts, White cell casts, Epithelial
cell cast
 The most common type of cast- hyaline casts are solidifiedTammHorsfall
mucoprotein secreted from the tubular epithelial cells and
seen in fever, strenuous exercise, damage to the glomerular
capillary.
 Red blood cells may stick together and form red blood cell casts.
Such casts are indicative of glomerulonephritis, with leakage of
RBC's from glomeruli, or severe tubular damage
 White blood cell casts are most typical for acute pyelonephritis,
but they may also be present with glomerulonephritis.Their
presence indicates inflammation of the kidney.
Microscopic examination of urine
Granular CastHyaline Cast
Microscopic examination of urine
A variety
of normal
and
abnormal
crystals
may be
present in
the urine
sediment
Chemical analysis of urine
 The chemical analysis of urine us undertaken to evaluate the
levels of the following componen:
 Protein
 Glucose
 Ketones
 Occult blood
 Bilirubin
 Urobilinogen
 Bile salts
Chemical analysis of urine
 The presence of normal and abnormal chemical elements in
the urine are detected using dry reagent strips called
dipsticks.
 When the test strip is dipped in urine the reagents are
activated and a chemical reaction occurs.
 The chemical reaction results in a specific color change.
 After a specific amount of time has elapse, this color change is
compared against a reference color chart provided by the
manufacturer of the strips.
Chemical analysis of urine
The dipstick method of chemical analysis
of urine
Chemical analysis of urine
Proteins in urine:
 Detected by heat coagulation or dipstick method
 Urine proteins come from plasma protein andTommHorsfall
(T-H) glycoprotein
 healthy individuals excrete <150 mg/d of total protein
and <30 mg/d of albumin.
 Plasma cell dyscrasias (multiple myeloma) can be
associated with large amounts of excreted light chains in
the urine, which may not be detected by dipstick.The
light chains produced from these disorders are filtered by
the glomerulus and overwhelm the reabsorptive capacity
of the proximal tubule and Bence Jones proteinuria
occurs
Chemical analysis of urine
Proteins in urine
 Normal- upto 150 mg/24 hours or 10mg/100ml in single
sample.
 Methods
Heat and acetic acid test- The test is based on the principle
of heat coagulation and precipitation of proteins by acetic acid.
 Sulphosalicylic acid test- Sulphosalicylic acid neutralizes
protein cation, resulting in precipitation of protein.
Causes of proteinuria
 Pre-renal
Addison’s disease
Fever
Eclampsia
Hypertension
Haemoglobinuria
Rhabdomyolysis
• Post renal
Lesions of renal pelvis, urethra (cystitis, prostatitis)
Severe UTI
Renal
All cases of
glomerulonephritis
Nephrotic
syndrome
Pyelonephritis
DAILY PROTEIN EXCRETION CAUSE
0.15 to 2.0 g Mild glomerulopathies
Tubular proteinuria
Overflow proteinuria
2.0 to 4.0 g Usually glomerular
> 4.0 g Always glomerular
Cause of Proteinuria as Related to
Quantity
 MINIMAL PROTEINURIA (<0.5 gm/day)
Exercise
Fever
Emotional stress
HTN
Renal tubular dysfunction
Polycystic kidneys
Lower UTI
 MODERATE PROTEINURIA (0.5-3 gm/day)
 Chronic glomerulonephritis
CCF
Pyelonephritis
Pre-eclampsia
Multiple myeloma
 MARKED PROTEINURIA (> 3gm/day)
Acute glomerulonephritis
Chronic glomerulonephritis, severe
Nephrotic syndrome
Diabetic nephropathy, severe
Renal amyloidosis
Lupus nephritis
TYPE
PATHOPHYSIOLOGIC
FEATURES CAUSE
Glomerular Increased glomerular
capillary permeability
to protein
Primary or
secondary
glomerulopathy
Tubular Decreased tubular
reabsorption of
proteins in glomerular
filtrate
Tubular or
interstitial disease
Overflow Increased production
of low-molecularweight
proteins
Classification of Proteinuria
Glomerular
Primary glomerulonephropathy
Minimal change disease
Idiopathic membranous
glomerulonephritis
Focal segmental
glomerulonephritis
Membranoproliferative
glomerulonephritis
IgA nephropathy
Selected Causes of Proteinuria by Type
Secondary glomerulonephropathy
Diabetes mellitus
Collagen vascular disorders (e.g.,
lupus nephritis)
Amyloidosis
Preeclampsia
Infection (e.g., HIV, hepatitis B and
C, poststreptococcal illness, syphilis,
malaria and endocarditis)
Gastrointestinal and lung cancers
Lymphoma, chronic renal
transplant rejection
Glomerulonephropathy associated with the following drugs:
Heroin
NSAIDs
Gold components
Penicillamine
Lithium
Heavy metals
Tubular
Hypertensive nephrosclerosis
Tubulointerstitial disease due to:
Uric acid nephropathy
Acute hypersensitivity
interstitial nephritis
Fanconi syndrome
Heavy metals
Sickle cell disease
NSAIDs, antibiotics
Overflow
Hemoglobinuria
Myoglobinuria
Multiple myeloma
Amyloidosis
 Selective proteinuria
 When LMW proteins like albumin (MW- 66000) or
transferrin (MW-76000) are selectively excreted through
kidney.
 Eg- all causes of nephrotic syndrome.
 Non-selective proteinuria
 When HMW protein like globulin, fibrinogen in addition to
LMW protein are excreted through kidney
Proteins in urine
 Heat and Acetic Acid Method
 Procedure :
 Take a long test tube and fill ¾ the tube with clear urine.
 Boil the upper portion over a flame, the lower portion serves as the
control.
 If proteins, phosphates or carbonates are present in the urine a turbidity
develops.
 Add 1-3 drops of 10% glacial acetic acid.
 Any turbidity due to phosphate precipitation will clear or if it is due to
carbonates they disappear with effervescence.
 If it persists, it is due to albumin.
Interpretation
 Negative – No turbidity or cloudiness.
 Trace – Cloudiness visible against a black background ( 5 mg /
dl).
 1+ - Definite cloudiness without flocculation and granularity
( 10 – 30 mg / dl ).
 2+ - Heavy and granular cloudiness without flocculation.
( 40 – 100 mg / dl).
 3+ - Dense opaque cloud with marked flocculation
( 200 – 500 mg / dl) .
 4+ - Thick cloudiness with precipitation
(  500 mg / dl ).
Sulphosalicylic acid test
 If urine is alkaline, it should be acidified.
 Procedure:
 2ml of acidic urine taken in test tube.
 Add an equal volume of 20% Sulphosalicylic acid.
 Mix thoroughly, allow it to stand for 10 minutes and
estimate the amount of turbidity.
 Absence of cloudiness- Absence of protein.
 If turbidity persists after boiling- Positive for
protein.
 Negative : No cloudiness
 Trace: Barely visible cloudiness.
 1+ : definite cloud without granular flocculation
 2+ : heavy and granular cloud without granular
flocculation
 3+ : dense cloud with marked flocculation.
 4+ : Cloudiness with precipitation
Quantitative estimation of protein
 Esbach’s method using albuminometer.
 Reagents
Esbach’s reagent
 Acetic acid
 pH paper
 Instrument
 Esbach’s albuminometer
Picric acid
Citric acid
Water
 Procedure
Fill Esbach’s albuminometer with
acidic urine upto mark U
and reagent is added upto mark R.
• Tube is shaken well by inversion.
• Stopper the tube.
• Keep in standing erect position for 18-24 hours for the precipitate
to settle down.
• Reading of the length of ppt is taken indicated by markings present
over the tube.
• Albumin is expressed in gm/L of urine.
 When test done on 24 hours urine sample, quantity of
urine passed per day may be calculated by
 Dividing quantity of albumin per litre by total quantity of
urine passed in 24 hours in litre.
Microalbuminuria
 Urinary albumin excretion between 30-300 mg/day.
 Cannot be detected by dipstick methods.
 Strong predictor of development of diabetic nephropathy.
 Can be detected 10-15 years before development of diabetic
nephropathy.
 Significant risk marker of cardiovascular ds.
 Measured by nephelometry and radioimmunoassay
Diagnostic relevance microalbuminuria
 In diabetic patients for early diagnosis of nephropathy.
 In hypertensive patients as indicator of end organ
damage
Bence Jones proteins
 BJ protein is abnormal LMW globulin consisting of light chains
of Ig either Lambda or Kappa chains.
 Characteristic feature- PPT at 400 C to 600 C and redissolves
at higher temperature (1000c) & reappears when the urine is
cooled.
 Conditions a/w BJ proteinuria:
 Multiple myeloma
 Plasmacytoma
 Waldesnstrom macroglobinaemia
Detection of Bence-Jones protein
 Take 5ml urine in a test tube.
 If the urine is cloudy, than filter it with filter paper.
 If the reaction is alkaline of urine than do it acidic by adding a few drops
of 25% acetic acid.
 Than set the test tube in a water bath.
 Heat in water bath for 15 minutes.
 If the Bence -Jones Protein is present in urine then precipitate forms
between temperature of 40°C -60°C.
 But when temperature is raised to 850 -100°C, precipitate disappears.
 When the temperature is decreased to 60°C, precipitate reappears.
 It again disappears when temperature goes below 400C.
SUGARS IN URINE
 This is a non-specific test useful for semiquantitation of
marked glucosuria.
 Benedict’s qualitative test
 Principle- Aldehyde group of reducing sugar reduces Cupric
ions in Benedict’s reagent to cuprous oxide.
 Detects all sugars except sucrose.
 The final color of the solution depends on how much of
this precipitate was formed, and therefore the color
gives an indication of how much reducing sugar was
present.
 Increasing amounts of reducing sugar
 Green yellow orange red
Components of Benedict’s reagent
 Sodium carbonate- 100 gm (Provides alkaline conditions
which are required for the redox reaction)
 Sodium citrate- 173 gm (complexes with the copper (II)
ions so that they do not deteriorate to copper(I) ions during
storage)
 Copper sulphate- 17.3 gm
 Procedure
 Take 5ml of Benedict’s reagent
 Boil for 3 – 5 minutes
 Add 0.5ml (8 drops)of urine.
 Boil for 2 minutes.
 Cool and note the colour.
 Recording results
 The color varies from blue through green – yellow- orangebrick
red.
Negative No change in color.
Trace Greenish blue
1+ Greenish yellow (0.5% sugar)
2+ Yellow (1% sugar)
3+ Orange precipitate (1.5% sugar)
4+ Brick red precipitate (2% sugar)
 Sugars detected by Benedict’s test-
Glucose
Galactose
Lactose
Fructose
Maltose
Pentose
 False +
Ascorbic acid, Creatinine, Uric acid
Salicylates
X-ray contrast
COLORIMETRIC REAGENT STRIP TEST
 Principle: this test is based on a double sequential enzyme
reaction.
 One enzyme, glucose oxidase, catalyzes the formation of
gluconic acid and hydrogen peroxide from the oxidation of
glucose.
 A second enzyme, peroxides catalyzes the reaction of
hydrogen peroxide with potassium iodide chromogen to
oxidize the chromogen to colors ranging from green to
brown.
KETONES IN URINE (ketonuria):
 TYPES
 Acetone, diacetic acid (acetoacetic acid),
betahydroxybutyric acid.
 Causes of Ketonuria:
DKA
Fever
Anorexia
Gastrointestinal disturbances
Fasting
Starvation
Severe vomiting
 Rothera’sTest for Acetone and Acetoacetic
Acid:
 Principle:
 Acetone and acetoacetic acid develops purple coloured
complex with sodium nitroprusside in alkaline medium.
 Hart’s test
 For detection of beta-hydroxybutiric acid.
 Rothera’sTest for Acetone and Acetoacetic
Acid:
 Procedure:
 Take 5ml of urine in a test tube and saturate it with
ammonium sulphate.
 Add 1 crystal of sodium nitroprusside.
 Mix.
 Run liquid ammonia carefully at the side of the tube so as to
form a layer on top of the saturated urine.
 POSITIVE- Formation of purple ring at junction of two
fluids.
OCCULT BLOOD IN URINE:
 Red blood cells / haemoglobin.
 Haematuria- when 5 or more intact RBCs/HPF.
Causes of Haemoglobinuria
 Malaria- black water fever.
 Hemolytic streptococcal septicaemia.
 Incompatible blood transfusion.
 Drugs- Sulphonamides, phenylhydralazine.
 PNH
Causes of Haematuria
 Renal
 Neoplasms
 Calculi
 TB
 Pyelonephritis
 Hydronephrosis
 Oxaluria
 Acute GN
 Polycystic kidney ds
 Post-Renal
 Ureter- calculus, neoplasm
 Urinary bladder- neoplasm,TB,
Cystitis, calculus.
 Prostate- BPH, Neoplasm
• General
 Embolism of kidney from SBE.
 Malignant HTN kidney
 Haemophilia
 Leukemia
Benzidine Test
 PRINCIPLE
 The peroxidase activity of hemoglobin decomposes hydrogen
peroxide releasing nascent oxygen which in turn oxidizes
benzidine to give blue color.
 REAGENTS
 A: Saturated solution of benzidine in glacial acetic acid
 B: Hydrogen peroxide
Benzidine Test
 PROCEDURE
 Add 2 ml of urine in test tube.
 Add 2ml of 1% Benzidine solution in acetic acid.
 Shake well.
 Add 2ml of hydrogen peroxide.
 Mix and observe for a change in color.
 Positive result: Green or blue color.
(Hematuria)
BILIRUBIN METABOLISM
Bile salts
 Primary bile acids
 Cholic acid and chenodeoxycholic acid (CDCA)- synthesized
from cholesterol in the liver, conjugated with glycine or
taurine, and secreted into the bile.
 Secondary bile acids
 Deoxycholate and lithocholate, are formed in the colon as
bacterial metabolites of the primary bile acids.
 Sodium taurocholate and sodium glycocholate are found in
urine.
Tests for detection of bile salts
 HayTest
 Principle:
Bile salts when present decreases surface tension of urine.
 Procedure:
Take 10 ml of urine in beaker.
Sprinkle dry sulphur powder on the surface of the urine
 Results:
 If bile salts are present they sink to the bottom.
 Otherwise they float on the surface.
Bile pigments
 Normal urine-
Urochrome
Traces of Urobilin
 Abnormal urine
Bilirubin
Urobilinogen
Biliverdin
Urobilin
Fouchets Test/Harrison’s spot test
 FOUCHETS REAGENT
 Trichloroacetic acid – 25 gms
 Distilled water - 100 ml
 10% Ferric chloride solution – 10 ml.
Principle:
 Barium chloride added to urine combines with sulphate radicals in urine
to form precipitate of barium phosphate. If bile pigments are present in
urine, they will adhere to these large molecules. Ferric chloride present
in fouchet reagent then oxidizes yellow bilirubin in presence of
trichloroacetic acid to green bilverdin.
Fouchets Test/Harrison’s spot test:
 PROCEDURE
 Place 5 ml of acidified urine in a test tube.
 Add 5ml of 10 % barium chloride.
 Mix and filter through filter paper.
 Let the paper dry.
 Add 1-2 drops of Fouchet’s reagent to the ppt on filter
paper.
 RESULT:A green color indicates the presence of
bilirubin.
Ehrlich’s test for urobilinogen
 Principle
Urobilinogen reacts with p-dimethylamino-benzaldehyde
to form red colour.
 Intensity of red colour is proportional to the concentration
of urobilinogen in urine.
 Reagents
P-dimethylaminobenzaldehyde
 HCL
 DW
Ehrlich’s test for urobilinogen
 Procedure
 Add 1ml of Ehrlich’s reagent to 10 ml of urine in test
tube.
 Mix by inversion.
 Let stand for 5 minutes.
 RESULT
 Pink- Normal
 Dark red colour- Positive for urobilinogen.
Causes of increased urobilinogen
 Cirrhosis
 Haemolytic jaundice
 Paralytic enterocolitis
 Hepatic congestion
LABELLING
 Sample container-for identification of sample.
 Cytology requisition form-for identification
of individual patient sample.
CENTRIFUGATION
Basically of 2 types
I Normal.
 II Cytospin-A device that spins cells in a fluid
suspension .
 Drawbacks-distortion of cellular morphology due to air
drying artifacts and loss of cells by absorption
of fluid into the filter card.
 In this process, urine sample is taken in a conical
tube and centrifuge at a rate of 2000rpm for 10-15
minutes.
PAPANICOLAOU STAIN
 Done by two methods-
1 Automated stainer-- large scale slides.
Takes 30 minutes for staining.
2 Manual staining using copplin jarFor
small scale slides.
Takes less than 7 minutes to stain.
 Staining objectivesI
Well stained nuclear chromatin.
II Differential counterstaining i.e. staining the cytoplasm of
different cell types into different colours and intensity.
III Retaining cytoplasmic transparency.
Urine Cytology
 INTERPRETATION-
1 Normal-Normal constituents of urine.
2 Abnormal-Any variation from normalI
cellular components
II Acellular components.
CELLS derived from
Urothelial and its variants.
 Renal tubules.
 Adjacent organs-like prostrate.
 Cells extragenous to the urinary tract-RBCs.
Urine Cytology….
A Cells-
-Erythrocytes-Hematuria
-Leucocytes-Infective etiology
-Epithelial cells
B Casts-Hyaline
cast
-Red cell cast
-Granular cast
-Epithelial cast
-waxy cast
-Fatty cast
C Crystals-Some are common in Acidic urine
-Some are common in Alkaline urine
D Bacteria-Normal urine is free from bacteria.
E Yeast.
F Malignant cells.
G Artifacts.
CELLS
Erythrocytes
 usually appear as hourglass appearance.
 presence of red cells 1-2RBCs/HPF is not
considered abnormal.
 in hypotonic urine red cells swell up causing
lysis -releasing Hb in urine-lysed cells are
referred as ghost cells.
 when the red cells are swollen/crenated
sometimes mistaken forWBCs and yeast cells
 Normal up to 1-2WBCs/HPF.
 Larger than red cells and smaller than renal epithelial cells.
 Usually spherical- singly/clumps.
 Mostly neutrophils-presence of characteristics granules
and lobulation.
 Addition of 2%acetic acid to slide accentuated the nuclei
of cells.
 Presence of many white cells in clumps is strongly
suggestive of acute urinary tract infection.
Leucocytes
Epithelial cells
 Any site in genitourinary tract from PCT to the urethra or from
the vagina.
 Normally a few cells from these sites can be found.
 A marked increase indicates inflammation of that proportion of
urinary tract from which the cell is derived.
TYPES
 Renal tubular
 Transitional
 Squamous
Renal tubular epi. cells
 Larger than white cells
 Large round nucleus.
 May flat/ cuboidal/ columnar.
 Increase no indicates tubular
damage.
Transitional epithelial cells
 2 to 4 times larger than
white cells.
 Round/ pear shaped/
may have tail like
projection.
 Line the urinary tract
from pelvis of kidney to
upper portion of
urethra.
Squamous epithelial cells
 Line urethra and
vagina.
 Have little
diagnostic
significance.
Crystals
 Usually not found in fresh urine but appear when
urine strands for a while.
 Many of crystal found in urine have little clinical
significance except in case of metabolic disorders.
 Crystals are identified by their appearance and their
solubility characteristics.
TYPES
Acidic urine crystals
 Alkaline urine crystals
CRYSTALS IN ACIDIC URINE
 URICACID.
 AMORPHOUS URATES
 CALCIUM OXALATE
 CYSTINE
 LEUCINE
 TYROSINE
 SULPHA
CRYSTALS IN ALKALINE URINE
 TRIPLE PHOSPHATE
 CALCIUM CARBONATE
 CHOLESTROL
 Amorphous phosphates
 Ammonium biurate
Uric acid crystals
 Most characteristics
form are diamond or
rhombic prism.
 Presence of uric acid
crystals in urine is a
normal appearance.
 Increase in-gout
-AFI
-Chronic nephritis
-high purine
metabolism
Calcium oxalate crystals
 Octahedral or envelope shaped
crystal
 Can be present in normal urine
after ingestion of various
oxalate rich foods.
 Pathological- DM
-Liver disease
-Severe chronic renal
disease
Amorphous urates
 Urates salts of sod, pot.
and calcium
 Having a granular
appearance
 Present in urine as non
crystalline amorphous
forms.
 No clinical significance.
Hippuric acid crystals
 Elongated prism like.
 Rarely seen in urine.
 No clinical significance.
Cystine crystals
 Refractile hexagonal
plate swith equal or
unequal sides.
 Frequently have
layered or laminated
appearance.
 Soluble in ammonia.
 Can be detected
chemically by Sod-
cyanide-sod.
Nitropruside test.
 Always Pathological
(Cystinosis).
Leucine crystals
 Highly refractile having
spheroid with radical and
concentric striations.
 Clinically very significant.
 Maple syrup disease
 Serious liver disease
Tyrosine crystals
 very fine needle
likes occurring in
sheaves or clusters.
 Clinically
significance
 Severe liver disease
 tyrosinosis
Cholesterol
crystals
 large or flat
plates with
notched corners
 Presence of
excessive in
urine indicates
tissue breakdown
Sulfa drugs crystals
 precipitate as
sheets of needles
usually with
eccentric
binding
 May be history
of sulfa drugs
medication
Alkaline urine crystals
Triple phosphates crystals
prism like with three to
six sides
 Frequently found in
normal urine
 Pathological
-chronic pyelitis
-cystitis
-enlarged prostate
Amorphous phosphates
 granular
particles
with no
definite
shape
 No clinical
significance.
Calcium carbonate
 appearing as dumbbell or spherical or large
granular mass.
 No clinical significance.
Casts
 Presence of casts are frequently associated with
proteinuria.
 Have nearly parallel sides with rounded or blunts ends.
 Always renal in origin and indicates intrinsic renal
disease
 Casts are more or less circular with thicker in middle.
Red cells cast
 meaning renal hematuria
 Always pathological.
White cell cast
Granular casts
 degeneration of
cellular casts or
direct aggregation
of serum proteins.
 Almost always
indicate significant
renal disease.
 May be fine
granular or coarse
granular casts.
Epithelial cells casts
 result as statis and desquamation of renal tubular epithelial
cells.
 Indicates tubular injury.
Waxy casts
 smooth
homogenous
appearance.
 Results from
degeneration of
granular casts.
 Found in acute
and chronic renal
disease.
Fatty casts
 Appear as a
few fat
droplets or
compose
almost entirely
of fat droplets
of various
sizes.
 Found in fatty
degeneration
of tubular
epithelial.
Hyaline cast
 Damage to glomerular capillary membrane, fever, orthostatic
proteinuria, and emotional stress or strenuous exercise.
Bacteria
 When accompanied with white cells usually indicates UTI.
 Occurs as rod or chains or cocci.
Artifacts
Starch crystals Fibres
Parasites
Enterobius vermicularis Schistosoma
Haematobioum
Yeast
 Usually ovoid cells with
budding.
 Not dissolve in 2%acetic
acid solution and not
stained with Eosin.
Malignancy
 Urinary bladder
 Renal pelvis
 Kidney
 Ureter
 Adjacent organs.
Types
 Low grade papillary tumours.
 High grade papillary tumours.